Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease that profoundly impacts the quality of life of millions worldwide.[1] Characterized by persistent itching, eczematous lesions, and a compromised skin barrier, AD is driven by a complex interplay of genetic predisposition, environmental factors, and immune dysregulation.[2] Central to its pathogenesis is an exaggerated immune response, particularly involving T helper 2 cells (Th2), leading to the release of inflammatory cytokines such as interleukin‐4 (IL‐4) and interleukin‐13 (IL‐13) that exacerbate skin inflammation. This evidence concerns the gene IL4 and atopic eczema.